Transcript Figure 1 - Grupo Akros

First Advanced Virtual Course of Electrocardiology:
New frontiers for a century-old discipline.
Sociedad Latinoamericana de Estimulación Cardíaca
y Electrofisiología (SOLAECE)
Class 1 – Value of Eletrocardiogram in the 21st Century
Prof. Dr. Andres Ricardo Perez Riera M.D.Ph.D.
Disciplina de Cardiologia - Chefe do Setor de Eletrovetorcardiografia
Faculdade de Medicina do ABC Fundação do ABC
Santo André – São Paulo – Brasil
Value of Electrocardiogram in the 21st Century
Twelve-lead ECG and derived methodologies is still current in the 21st century as one of the first
pillars of cardiological diagnosis: the clinical pillar (interrogation and physical examination),
ECG and transthoracic echo. Figure 1. More than 95% of diagnoses in cardiology are made
without requiring other supplementary methods.
In spite of the centennial, it is still the basis of the supplementary rationale for cardiologists,
internists, family doctors, intensivists, in the ER and in pediatrics. There are several scenarios
where the ECG is the gold standard: when making a decision on the management before clinical
symptoms compatible with acute coronary syndrome. Figure 2. In this scenario, the presence or
not of ST segment elevation is a watershed for the indication of invasive study or just
pharmacological behavior. Figure 3
Decisive in the cases of heart failure refractory to proper medication and resynchronization
management. The following are predictive parameters of good response, sinus rhythm, absence of
P wave suggesting interatrial conduction disorder, pattern of complete left bundle branch block
with QRS duration ≥130 ms (men) and 140 ms (women). In the presence of hypertrophic or
dilated LV, the duration criteria for CLBBB (≥120 ms) presents a low specificity. Strict LBBB
criteria associated to notch in at least 2 leads in V1-V2 or V5-V5, I and aVL presents high
sensibility and specificity. Figures 4 and 5.
In the diagnosis of genetic channelopathies without structural heart disease, class 1 indication in
the diagnosis of syncope(1), in cardiomyopathies and myocarditis, congenital heart diseases and
in the identification of artifacts.
Figure 1
THE FIVE PILLARS OF CARDIOLOGICAL DIAGNOSIS
ECG
Physical examination
ECHO o chext X-ray
Lab tests
History
Fundamental in the diagnosis and management in the presence of arrhythmias. It allows to
identify the focus (supraventricular, junctional or ventricular) and offers a guide on therapy
(pharmacological, cardioversion, radiofrequency or hybrid).
Main scenarios in which ECG may be decisive or helpful for the
diagnosis and/or therapy
1. In acute coronary syndrome. Figures 2 and 3
2. In indication of cardiac resynchronization in the case of refractory
CHF
3. In symptoms of syncope (class I indication)
4. In arrhythmias
5. In the diagnosis of inherited channelopathies
6. In the diagnosis of cardiomyopathies and myocarditis
7. In the clinical and epidemiological screening of chronic chagasic
myocarditis
8. In electrolytic disorders and effect of drugs
9. In acyanotic and cyanotic congenital heart diseases
10.In the identification of artifacts.2
Figure 2
Chest pain causes
Cardiac causes
Ischemic
Stable
Angina
≈ 5%
of total
Non-cardiac causes
Non-ischemic
Unstable
Angina
Acute
Myocardial
Infarction
Gastroesophageal
Gastroesophageal
Reflux
Esophageal
spasm
Nongastroesophageal
Peptic Ulcer
Acute Coronary Syndrome
Valvular
Pericarditis
Acute aortic
dissection
Pneumothorax
Acute Pulmonary
Embolism
Muscle/skeletal
Psychoemotional
Figure 3
Acute Coronary Syndome
ELECTROCARDIOGRAM
STEMI
> 2 mm in V1, V2 or V3 or > 1 mm in other leads
Q- wave AMI
Non-Q AMI
New LBBB
True posterior
AMI pattern
Thrombolytics or primary coronary angioplasty
* Actual basal inferior.
NSTEMI
*
NEGATIVE
BIOMARKERS
POSITIVE
BIOMARKERS
Unstable
Angina
Non-Q AMI
Figure 4
Multisite Cardiac Resynchronization:
Relevant Electrocardiographic Aspects
Figura 5
There are 2 types of implantable devices for CHF: Multisite resynchronization pacemaker with leads in
the LV, RV and RA, called CRT. There is a more complete modality that associates automatic
cardioverter defibrillator (CRT-D). Both devices help to coordinate the pump function of the heart and
to improve blood flow. They improve the performance of the pump by increasing systolic discharge.
Electrocardiographic factors associated to low ejection fraction in the presence of CLBBB
The following ECG parameters are associated to low EF in the presence of CLBBB.
1. P wave of duration ≥120 ms
2. Final negative component of P wave in V1 with positive Morris criteria (deep and slow)
3. QRS electrical axis in the frontal plane with extreme shift to the left (>30º) or right (>+90º)
4. QRS duration ≥160 ms
5. Deep S waves in V3-V4
6. Notches in inferior leads.
The presence of 2 or 3 or these alterations present PPV of 98.0% and NPV of 60.4% for
reduced LVEF(2).
Markers of good response in cardiac resynchronization
1. Epidemiological: female gender
2. Non-ischemic etiology
3. Electrocardiographic: CLBBB pattern with duration ≥150 ms for at least >120-130 ms because it is
considered a marker of electrical and mechanic dyssynchrony with exceptions. The pattern and QRS
duration is the only parameter that should be used according to randomized studies.
4. ECG QRSd ≥140 ms for men or ≥130 ms for women associated to middle notch in QRS, in at least 2
leads, I, aVL, V1, V2, V5, and/or V6. (3)
5. QRS >150 ms are the ones that benefit the most with CRT
6. fQRS presents a sensibility of 93% and specificity of 90% respectively, to locate the segment with
dyssynchrony.
7. Biventricular pacing by stimulating the area with greatest delay(4)
8. Choose the site of greater mechanic delay by transvenous approach in tributary veins of the coronary
sinus (rate of success, 90%). The site of greatest delay is evaluated by speckle-tracking imaging in the
latero-dorsal wall.
Markers of poor response in cardiac resynchronization therapy
1) Male gender(5)
2) CRBBB pattern
3) Narrow QRS complex
4) Co-morbidities
•
CRF: creatinine clearance < 30ml/min/m2
•
Chronic obstructive pulmonary disease (COPD)
•
Anemia
•
Pulmonary hypertension
5) Coronary artery disease
6) Significant cardiomegaly
7) Previous LVEF ≤23%(1)
8) Previous functional class IV(1)
9) Ischemic patients with previous acute myocardial infarction(6)
10) LV end diastolic diameter >75 mm: severely dilated and remodeled ventricles.
11) Severe mitral valve insufficiency
12) Scars in the area of electrode implant (high thresholds) or large scars affecting >50% of the LV.
13) Inappropriate programming of AV and VV intervals. With mitral annular tissue Doppler, separation of
E/A with AV interval optimization.
Cardiac resynchronization therapy is a significant therapeutic modality in symptomatic patients with heart
failure refractory to drugs with CLBBB pattern and wide QRS (≥120 ms) in the electrocardiogram. However,
regrettably wide QRS (considered as a marker of electrical dyssynchrony) is present in just 30% of the
patients with heart failure, which turns most of the patients with heart failure refractory to drugs, non-eligible
for resynchronization therapy.
A significant number of patients with narrow QRS presents echocardiographic evidence of left ventricular
dyssynchrony. However, there are few data on the additional resources in surface ECG that may predict
intraventricular dyssynchrony.
Fragmented QRS (fQRS) is a marker of electrical dyssynchrony, which results in significant intraventricular
dyssynchrony in patients of non-ischemic dilated cardiomyopathy and narrow QRS interval. fQRS locates the
dyssynchronous segment and may be useful in the identification of patients that may benefit from cardiac
resynchronization therapy(7)
Value of ECG in the diagnosis of channelopathies without apparent structural heart
disease.
Brugada syndrome: The diagnostic confirmation is only possible in the presence of type 1 pattern: ST
segment elevation ≥2 mm, of upper convexity or descending oblique rectilinear followed by negative T in
the right precordial leads (V1-V2 or from V1 through V3) and/or high right leads V1H, V2H and V3H (they
increase diagnostic sensibility). Figure 6.
Figure 6
Typical type 1 Brugada pattern in the right precordial leads V1 and V2
Long QT syndrome: The LQT1 variant is characterized by wide-base T waves, moderate QT
dependence on heart rate modifications and paradoxical prolongation of QT with infusion of low
doses of epinephrine. LQT2 is characterized by bifid T waves (T1-T2 >150 ms),
In LQT3, prolonged QT interval by greater ST segment duration and late appearance of T. Figure
7.
Figure 7
LQT1
LQT2
LQT3
Short QT syndrome: very short intervals, J point interval to the apex of T <120 ms: Jp-Tp (1
point)(2) and prolonged Tpeak/Tend (Tpe) >94 ms in men and >92 ms in women when measured
in V5, frequent early repolarization, T wave of great voltage, narrow base and high tendency to
atrial fibrillation. Figure 8.
Figure 8
Minus-plus T-wave signal
. Very Short QT interval. ST segment is absent or minimal, tall peaked pseudosymmetric T wave
or hyperkalemic-like T wave
Catecholaminergic polymorphic ventricular tachycardia. Recurrent syncopes, triggered by
physical or emotional stress, consequence of polymorphic VT. In the latter, QRS axis changes
from beat to beat from -60º to +120º from and in precordial leads; alternating pattern of LBBB
and RBBB. Figure 9.
Figure 9
Female, white, 20-year-old patient; recurrent syncope of uncertain etiology after physical and emotional
stress, carrier of familial catecholaminergic cardiomyopathy. Alternating QRS complexes are observed with
alternating right and left bundle branch block morphology. The QRS axis shifts from –60º to +120º.
In the diagnosis of cardiomyopathies and myocarditis
In the diagnosis of hypertrophic cardiomyopathy
ECG presents a greater sensibility than auscultation and echocardiogram in the detection of hypertrophic
cardiomyopathy, main cause of sudden cardiac death between athletes younger than 35 years old; i.e. when
the auscultation is negative and normal echocardiogram, ECG may raise the suspicion of existence of
hypertrophic cardiomyopathy(8). Figure 10.
Figure 10
HCM, non-obstructive form. Apical portion of the septum with 32 mm of diastolic thickness. LAE
LVE, systolic pattern by significant secondary alteration of ventricular repolarization in antero-lateral and
inferior wall.
In the diagnosis of arrhythmogenic RV cardiomyopathy/dysplasia
Approximately 90% of carriers present altered ECGs, and in follow-up, no ARVC/D presents
normal ECG at six years. The following are major criteria: presence of epsilon waves, inverted T
waves in right precordial leads >14 years in absence of RBBB and recording of monomorphic
VT with pattern of CLBBB and superior axis; duration V1+ V2+ V3 / V4+ V5+ V6 . ≥ 1.2, QRS
duration from V1 to V2 >110 ms in absence of RBBB and prolongation of ascending ramp of S
from V1 through V3 in absence of RBBB(9). Figure 11
Typical example of ECG of ARVC/D
Figure 11
Sinus rhythm, complete RBBB, terminal notch located in the J point J (EPSILON wave). EPSILON wave
would be the result of delayed activation in the RV, and visible from V1 through V3 and in the frontal plane
leads. T wave inversion is observed in V1 through V3 characteristic of ARVC/D.
In the clinical and epidemiological screening of chronic chagasic myocarditis
In all of Latin America, the electrocardiographic pattern characterized by association of CRBBB
+ LAFB and polymorphic premature ventricular contractions in patients from endemic area,
should raise the suspicion of American trypanosomiasis.
The next example presents the mentioned characteristics. Figure 12.
Figure 12
In congenital heart diseases
Tumultuous, brief, RV impulse with wide fixed split second heart sound, no murmurs 3/6 + in
pulmonary focus in the 2nd intercostal space, and ECG with pattern of IRBBB or CRBBB,
suggesting ASD-OS. Figure 13.
Figure 13
Child with Down syndrome, fremitus and systolic murmur of mitral valve insufficiency, ejection
mumur in pulmonary focus and wide and fixed split second sound, with ECG pattern of RBBB +
LAFB + BVE is very suggestive of ASD-OP or endocardial cushion defect. (10). Figure 14.
Figure 14
DI
V4R
DII
V1
V2
DIII
aVR
aVL
V3
V4
V5
aVF
V6
First degree AV block, biventricular enlargement, right bundle branch block and left anterior fascicular block. First
degree AV block + BVE + CRBBB + LAFB
Cyanotic, hypoxic infant, with possible non-circular pupil, associated to RAE, P of Gamboa
pattern + diastolic LVE + extreme axis shift to the left, strongly suggesting tricuspid atresia.
Figure 15.
Figure 15
RAE: Visible in V2 and with notch in the ascending ramp of P wave.
LVE: Deep S in V1 and R of increased voltage in V5. In V6, it resembles ILBBB.
LAFB: AQRS with extreme shift in the left upper quadrant and counterclockwise rotation in the FP.
qR in DI and aVL. rS in inferior leads.
Giant P wave + bizarre RBBB of low voltage or WPW, suggesting Ebstein’s anomaly.(11)
Systolic murmur in the mesocardium associated to wide isodiphasism in intermediate precordial leads:
(Katz-Wachtel sign) of BVE suggesting VSD(12). Figure 16.
Figure 16
Katz-Walchtel ECG sign or phenomenon
Isodiphasic wide QRS in intermediate precordial leads. It indicates biventricular enlargement/hypertrophy
Q wave >40 ms in children in the apical or lateral wall, suggesting anomalous origin of the
coronary artery; one of the important causes of sudden cardiac death in young athletes.
Negative P wave in I and positive in aVR, deep Q wave in I and aVL, progressively smaller QRS
complexes from V1 through V6 indicating Dextrocardia. Figure 17.
Figure 17
Clinical diagnosis: True simple dextrocardia: mirror image. Total atrio-visceral situs inversus without heart disease.
ECG diagnosis: SAP to the right and below, pointing at around +1200 ( DIII). Negative P wave in aVL and DI, positive in DIII.
Reverse progression of r wave in precordial leads. V2 through V5 (decreasing).
CONCLUSION: True Dextrocardia.
Independence of P and QRS, narrow QRS with low HR, suggesting congenital complete AV
block. Figure 18.
Figure 18
In the identification of artifacts
Electrical interference: baseline with oscillations. Cause: poor ground connection; inappropriate cleaning
of the skin; baseline oscillations; limbs movement: sudden irregularities of the baseline: children or
neurological patients with involuntary movements, Parkinson’s tremor. It may resemble VT (3) or atrial
flutter. The placement of electrodes in the origin of the limbs decreases the interference caused by
myopotentials.
Exchange of limb electrodes resembling dextrocardia; however, precordial progression is normal.
Exchange of precordial electrodes; incorrect placement. In case of a daltonic technician, he/she may
exchange V1 (red) by V3 (green) or placement at an upper or lower level. And the great precordial
electrode: by using conductive gel in the band: tracing recording equal from V1 through V6(13). Figure
19.
Figure 19
Parkinson’s tremor that resembles ventricular tachycardia
Limitations
1.
2.
3.
4.
5.
6.
7.
8.
9.
It may be dangerous if we trust too much in a normal ECG and ignore the clinical context;
The presence of normal ECG does not rule out the presence of severe CAD
There are infarctions without the presence of Q wave and without ventricular repolarization alterations;
It presents a low sensibility in the diagnosis of ventricular enlargement;
Normal ECG does not mean “life is guaranteed”;
It is extremely important to bear in mind the existence of false positives and false negatives;
In the release for the practice of sports, a normal ECG does not mean absence of risk. A release without
another more accurate test, such as ergometer test or echocardiogram will depend on the clinical
context;
The presence of factors that may influence the ECG should always be considered, such as: gender,
weight, ethnical group, body type, chest deformities (pectus excavatus, mastectomized straight back),
competitive practice of sports, hypothermia, hyperventilation, injection of glucose, ingestion of alcohol,
etc;
Presence of artifacts: tremor, Parkinson, young children, accidental electrode exchange, poor
standardization (damping), inappropriate paper speed.
Conclusions
In all cases, the interpretation of ECG should take into account the
clinical context, as any other supplementary method and it should be
interpreted by an experienced physician.
The method is still decisive in several clinical scenarios, when making
a diagnosis or in management.
Rest ECG. Levels of evidence to indicate it.
Patients with known cardiovascular disease or dysfunction
Class I

As initial evaluation;

Patients in whom the pharmacological treatment may produce electrocardiographic alterations
correlated with therapeutic response or progression of the disease;

Patients in whom the pharmacological treatment may produce adverse effects that may be predicted or
detected by alterations in ECG.

Patients with changes in symptoms, signs or relevant lab findings;

Patients with permanent pacemaker or cardioverter defibrillator;

As pre-operative evaluation;

Patients with syncope or pre-syncope;

Patients with changes in pattern of chest pain;

Precordial pain;

Initial dyspnea or worsening of NYHA functional class;

Extreme unexplained fatigue, weakness or prostration;

Presence of murmur;

Presence of friction;

Complaint of palpitations;

Appearance of new signs of CHF;

Signs that suggest pulmonary hypertension;

Poorly controlled or accelerated hypertension;

Evidence of recent stroke;

New episode of arrhythmia or abnormal ventricular rate;
Rest ECG: Levels of evidence to perform it
Patients with known cardiovascular disease or dysfunction
Class II

Pre-operative period of hemodynamically stable patients with non-significant heart disease, mild
hypertension and infrequent PVCs.
Class III

Patient with benign heart condition as mitral valve prolapse and mild hypertension;

Adult patients with stable chronic heart disease, seen at intervals of 4 months or less, and with no new
or unexplained findings.
Patients in risk of developing cardiovascular disease or dysfunction
Class I

Users of cocaine, amphetamines or any other illicit drug;

Excessive dose of drugs with effects on the heart;

Use of antineoplastic agents, lithium, AIDS drugs, and antidepressants.
Class II

To evaluate the response to the administration of a drug that may knowingly cause electrolytic
alteration;
Class III

To evaluate the response to administration of a drug known not to affect cardiac function.
Rest ECG: Level of evidence to perform it
Patients without suspected heart disease or dysfunction
Class I
•
•
People older than 40 that undergo medical examination;
Before the administration of antineoplastic drugs (high incidence of adverse effects);
Criteria to confirm or classify a preliminary diagnosis of cardiac dysfunction
I) Cardiomyopathy characterized by LVEF decrease, global or more severe in the septum
II) Symptoms associated to HF.
III) Signs associated to HF, such as S3 gallop, tachycardia, or both
IV) Reduction of LVEF of at least 5 for less than 55% with signs or symptoms of HF, or drop of LVEF
of at least 10 for less than 55%, without sings of symptoms.
•
•
People of any age, whose job requires an optimal cardiovascular state: Policemen, pilots, drivers, firemen,
air traffic controller, elite athletes;
People with more than 40 years, as pre-operative evaluation;
•
People evaluated as heart transplant donor or receptor of non-cardiac transplant.
References
1. Huff JS, Decker WW, Quinn JV, et al. Clinical policy: critical issues in the evaluation and
management of adult patients presenting to the emergency department with syncope. Ann Emerg.
Med. Apr 2007; 49: 431-444.
2. Rodrigues de Oliveira Neto N et al Correlação entre eletrocardiograma e função sistólica na
presença de bloqueio de ramo esquerdo. Relampa 2012; 25: 91-98.
3. Galeotti L,et al. Evaluating strict and conventional left bundle branch block criteria using
electrocardiographic simulations. Europace. 2013 Dec;15(12):1816-21)
4. Bax JJ et al. Echocardiography and non invasive imaging in cardiac resyncrhornization
therapy;results of the PROSPECT(Predictors of Response to Cardiac Resynchronization Therapy)
Study on perspective J Am Coll Cardiol 2009; 53: 1933-43.
5. Zayas Molina R et al Terapia de resincornización con marcapasos biventriculares. Evaluación a los
5 años de seguimiento. Relampa 2012; 25: 99-106)
6. Van Bommel RJ et al Characteristics of heart failure patients associated with good and poor
response to cardiac resynchronization theraphy: a PROSPECT( Predictor of Response to CRT)
sub-analysis. Eur Heart J 2009; 30: 2470-2477.)
7. Yusuf J et al Fragmented narrow QRS complex: Predictor of left ventricular dyssynchrony in nonischemic dilated cardiomyopathy.Indian Heart J. 2013 Mar-Apr;65:172-179.
8. Pérez-Riera AR, de Lucca AA, Barbosa-Barros R,Yanowitz FG de Cano SF, Cano MN, PalandriChagas AC. Value of electro-vectorcardiogram in hypertrophic cardiomyopathy. Ann Noninvasive
Electrocardiol. 2013 Jul;18(4):311-26
9. Nasir K, Bomma C, Tandri H, Roguin A, Dalal D, Prakasa K, Tichnell C, James C, Spevak
PJ, Marcus F, Calkins H. Electrocardiographic features of arrhythmogenic right ventricular
dysplasia/cardiomyopathy according to disease severity: a need to broaden diagnostic criteria.
Circulation. 2004; 110:1527-1534.
10. Caro M, Conde D, Pérez-Riera AR, de Almeida AP, Baranchuk A.The electrocardiogram in Down
syndrome. Cardiol Young. 2014 Apr 2:1-7.
11. Muñoz-Castellanos L, Espinola-Zavaleta N, Kuri-Nivón M, Keirns C. Ebstein's Anomaly:
anatomo-echocardiographic correlation. Cardiovasc Ultrasound. Nov 23 2007;5:43.
12. Katz LN and Wachtel H. The diphasic QRS type of electrocardiogram in congenital heart disease.
Am Heart J; 1937, 13: 202-206
13. Barake W, Baranchuk A, Pinter A. Pseudo-Ventricular Tachycardia Mimicking Malignant
Arrhythmia in a Patient with Rapid Atrial Fibrillation Am J Crit Care. 2014 May;23(3):270-272.